Histamine triggers microglial responses indirectly via astrocytes and purinergic signaling

Xia, Peng‐Fei; Logiacco, Francesca; Huang, Yimin; Kettenmann, Helmut; Semtner, Marcus

doi:10.1002/glia.24039

Cited by 18 publications

(9 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To this end, we have previously demonstrated sexually dimorphic differences between male and female Nf1 ± neurons [15], which reflect sex by genotype effects on cyclic AMP generation and dopamine homeostasis. Additional studies will be necessary to determine whether differences in neuronal dopamine (or other paracrine factors) underlie the sexually dimorphic differences observed in microglia [2,19,39,40,64,69]. Understanding how this intercellular crosstalk is established and maintained will provide new insights into our understanding of sex differences and the interplay between risk factors and cellular function in the brain.…”

Section: Discussionmentioning

confidence: 99%

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

Logiacco

Grzegorzek

Cordell

et al. 2023

acta neuropathol commun

Self Cite

View full text Add to dashboard Cite

We previously discovered a sex-by-genotype defect in microglia function using a heterozygous germline knockout mouse model of Neurofibromatosis type 1 (Nf1 ± mice), in which only microglia from male Nf1 ± mice exhibited defects in purinergic signaling. Herein, we leveraged an unbiased proteomic approach to demonstrate that male, but not female, heterozygous Nf1 ± microglia exhibit differences in protein expression, which largely reflect pathways involved in cytoskeletal organization. In keeping with these predicted defects in cytoskeletal function, only male Nf1 ± microglia had reduced process arborization and surveillance capacity. To determine whether these microglial defects were cell autonomous or reflected adaptive responses to Nf1 heterozygosity in other cells in the brain, we generated conditional microglia Nf1-mutant knockout mice by intercrossing Nf1flox/flox with Cx3cr1-CreER mice (Nf1flox/wt; Cx3cr1-CreER mice, Nf1MG ± mice). Surprisingly, neither male nor female Nf1MG ± mouse microglia had impaired process arborization or surveillance capacity. In contrast, when Nf1 heterozygosity was generated in neurons, astrocytes and oligodendrocytes by intercrossing Nf1flox/flox with hGFAP-Cre mice (Nf1flox/wt; hGFAP-Cre mice, Nf1GFAP ± mice), the microglia defects found in Nf1 ± mice were recapitulated. Collectively, these data reveal that Nf1 ± sexually dimorphic microglia abnormalities are likely not cell-intrinsic properties, but rather reflect a response to Nf1 heterozygosity in other brain cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

Logiacco

Grzegorzek

Cordell

et al. 2023

acta neuropathol commun

Self Cite

View full text Add to dashboard Cite

show abstract

“…Microglia express purinergic receptors, such as P2X7, P2Y6, and P2Y12, whose downstream signal triggers microglial phagocytosis (Haynes et al, 2006 ; Koizumi et al, 2007 ; Rajbhandari et al, 2014 ). It is reported that activated astrocytes secreted ATP to enhance phagocytic activity of microglia via P2Y12 purinergic receptor (Figure 4b ) (Xia et al, 2021 ). Astrocyte‐derived ATP also assists microglial phagocytosis by acting as a chemoattractant for microglia to the site of phagocytosis.…”

Section: Interactive Regulation Between Astrocytes and Micro...mentioning

confidence: 97%

Phagocytic astrocytes: Emerging from the shadows of microglia

Konishi

Koizumi

Kiyama

2022

Glia

View full text Add to dashboard Cite

Elimination of dead or live cells take place in both a healthy and diseased central nervous system (CNS). Dying or dead cells are quickly cleared by phagocytosis for the maintenance of a healthy CNS or for recovery after injury. Live cells or parts thereof, such as the synapses and myelin, are appropriately eliminated by phagocytosis to maintain or refine neural networks during development and adulthood. Microglia, the specific population of resident macrophages in the CNS, are classically considered as primary phagocytes; however, astrocytes have also been highlighted as phagocytes in the last decade. Phagocytic targets and receptors are reported to be mostly common between astrocytes and microglia, which raises the question of how astrocytic phagocytosis differs from microglial phagocytosis, and how these two phagocytic systems cooperate. In this review, we address the consequences of astrocytic phagocytosis, particularly focusing on these elusive points.

show abstract

“…In addition, the excitatory neurotransmitter glutamate is released from astrocytes and has been reported to cause microglial activation in a TNF-α–dependent manner, resulting in neuroinflammation and unbalanced neurotoxicity ( 51 ). Histamine, a monoamine neurotransmitter, is known to regulate microglial histamine responses mediated by histamine receptor isoform 1, which is expressed mostly on astrocytes ( 52 ). These observations suggest that an unbalanced neurotransmitter system affects glial cross-talk ( Fig.…”

Section: Neuroinflammatory Interactions In the Nvu And Their Associat...mentioning

confidence: 99%

The link between neuroinflammation and the neurovascular unit in synucleinopathies

et al. 2023

View full text Add to dashboard Cite

The neurovascular unit (NVU) is composed of vascular cells, glial cells, and neurons. As a fundamental functional module in the central nervous system, the NVU maintains homeostasis in the microenvironment and the integrity of the blood-brain barrier. Disruption of the NVU and interactions among its components are involved in the pathophysiology of synucleinopathies, which are characterized by the pathological accumulation of α-synuclein. Neuroinflammation contributes to the pathophysiology of synucleinopathies, including Parkinson’s disease, multiple system atrophy, and dementia with Lewy bodies. This review aims to summarize the neuroinflammatory response of glial cells and vascular cells in the NVU. We also review neuroinflammation in the context of the cross-talk between glial cells and vascular cells, between glial cells and pericytes, and between microglia and astroglia. Last, we discuss how α-synuclein affects neuroinflammation and how neuroinflammation influences the aggregation and spread of α-synuclein and analyze different properties of α-synuclein in synucleinopathies.

show abstract

Histamine triggers microglial responses indirectly via astrocytes and purinergic signaling

Cited by 18 publications

References 54 publications

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

Phagocytic astrocytes: Emerging from the shadows of microglia

The link between neuroinflammation and the neurovascular unit in synucleinopathies

Contact Info

Product

Resources

About